Transcript Slide 1 - AccessPharmacy

Schematic model for physiologic control of hydrogen ion (acid) secretion by the parietal cells of the gastric fundic glands. Parietal cells are stimulated to
secrete acid (H+) by gastrin (acting on gastrin/CCK-B receptor), acetylcholine (M3 receptor), and histamine (H2 receptor). Acid is secreted across the
parietal cell canalicular membrane by the H+/K+-ATPase proton pump into the gastric lumen. Gastrin is secreted by antral G cells into blood vessels in
response to intraluminal dietary peptides. Within the gastric body, gastrin passes from the blood vessels into the submucosal tissue of the fundic glands,
where it binds to gastrin-CCK-B receptors on parietal cells and enterochromaffin-like (ECL) cells. The vagus nerve stimulates postganglionic neurons of
the enteric nervous system to release acetylcholine (ACh), which binds to M3 receptors on parietal cells and ECL cells. Stimulation of ECL cells by gastrin
Source: Chapter 62. Drugs Used in the Treatment of Gastrointestinal Diseases, Basic & Clinical Pharmacology, 12e
(CCK-B receptor) or acetylcholine (M3 receptor) stimulates release of histamine. Within the gastric antrum, vagal stimulation of postganglionic enteric
Citation:gastrin
Katzung
BG, Masters
AJ. Basic
& Clinical
Pharmacology,
12e; 2012 Available
at: http://mhmedical.com/
March
neurons enhances
release
directlySB,
by Trevor
stimulation
of antral
G cells
(through gastrin-releasing
peptide,
GRP) and indirectlyAccessed:
by inhibition
of
30,
2017
somatostatin secretion from antral D cells. Acid secretion must eventually be turned off. Antral D cells are stimulated to release somatostatin by the rise in
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McGraw-Hill
Education.
All rights
reserved
intraluminal H+
concentration
by CCK that
is released
into the
bloodstream by duodenal I cells in response to proteins and fats (not shown). Binding of
somatostatin to receptors on adjacent antral G cells inhibits further gastrin release. ATPase, H+/K+-ATPase proton pump; CCK, cholecystokinin; M3,